Multicellular organisms rely upon the movement of signaling molecules across cells, tissues and organs to communicate among distal sites. In plants, herbivorous insects, necrotrophic pathogens and mechanical wounding stimulate the activation of the jasmonate (JA) pathway, which in turn triggers the transcriptional changes necessary to protect plants against those challenges, often at the expense of growth. Although previous evidence indicated that JA species can translocate from damaged into distal sites, the identity of the mobile compound(s), the tissues through which they translocate and the consequences of their relocation remain unknown. Here, we demonstrated that endogenous JA species generated after shoot injury translocate to unharmed roots via the phloem vascular tissue in Arabidopsis thaliana. By wounding wild-type shoots of chimeric plants and by quantifying the relocating compounds from their JA-deficient roots, we uncovered that the JA-Ile precursor 12-oxo-phytodienoic acid (OPDA) is a mobile JA species. Our data also showed that OPDA is a primary mobile compound relocating to roots where, upon conversion to the bioactive hormone, it induces JA-mediated gene expression and root growth inhibition. Collectively, our findings reveal the existence of long-distance transport of endogenous OPDA which serves as a communication molecule to coordinate shoot-to-root responses, and highlight the importance of a controlled distribution of JA species among organs during plant stress acclimation.

Reduced height 8 (Rht8) is the main alternative to the GA-insensitive Rht alleles in hot and dry environments where it reduces plant height without yield penalty. The potential of Rht8 in northern-European wheat breeding remains unclear, since the close linkage with the photoperiod-insensitive allele Ppd-D1a is unfavourable in the relatively cool summers. In the present study, two near-isogenic lines (NILs) contrasting for the Rht8/tall allele from Mara in a UK-adapted and photoperiod-sensitive wheat variety were evaluated in trials with varying nitrogen fertiliser (N) treatments and water regimes across sites in the UK and Spain.The Rht8 introgression was associated with a robust height reduction of 11% regardless of N treatment and water regime and the Rht8 NIL was more resistant to root-lodging at agronomically-relevant N levels than the tall NIL. In the UK with reduced solar radiation over the growing season than the site in Spain, the Rht8 NIL showed a 10% yield penalty at standard agronomic N levels due to concomitant reduction in grain number and spike number whereas grain weight and harvest index were not significantly different to the tall NIL. The yield penalty associated with the Rht8 introgression was overcome at low N and in irrigated conditions in the UK, and in the high-temperature site in Spain. Decreased spike length and constant spikelet number in the Rht8 NIL resulted in spike compaction of 15%, independent of N and water regime. The genetic interval of Rht8 overlaps with the compactum gene on 2DS, raising the possibility of the same causative gene. Further genetic dissection of these loci is required.Abbreviations ANOVA, analysis of variance; Y, yield; HI, harvest index; GN, grain number (m−2); SS, spikelet number (spike−1); SN, spike number (m−2); HD, heading date; AN, anthesis; 12L, length of the second internode from the top; 13L, length of the third internode from the top; PAR, photosynthetically active radiation; R: FR, red: far-red light reflectance ratio; RCBD, randomised complete block design

Physical damage can strongly affect plant growth, reducing the biomass
of developing organs situated at a distance from wounds. These effects,
previously studied in leaves, require the activation of jasmonate (JA)
signalling. Using a novel assay involving repetitive cotyledon wounding
in Arabidopsis seedlings, we uncovered a function of JA in
suppressing cell division and elongation in roots. Regulatory JA
signalling components were then manipulated to delineate their relative
impacts on root growth. The new transcription factor mutant myc2-322B was isolated. In vitro transcription assays and whole-plant approaches revealed that myc2-322B is a dosage-dependent gain-of-function mutant that can amplify JA growth responses. Moreover, myc2-322B
displayed extreme hypersensitivity to JA that totally suppressed root
elongation. The mutation weakly reduced root growth in undamaged plants
but, when the upstream negative regulator NINJA was genetically removed,
myc2-322B powerfully repressed root growth through its effects
on cell division and cell elongation. Furthermore, in a JA-deficient
mutant background, ninja1 myc2-322B still repressed root
elongation, indicating that it is possible to generate JA-responses in
the absence of JA. We show that NINJA forms a broadly expressed
regulatory layer that is required to inhibit JA signalling in the apex
of roots grown under basal conditions. By contrast, MYC2, MYC3 and MYC4
displayed cell layer-specific localisations and MYC3 and MYC4 were
expressed in mutually exclusive regions. In nature, growing roots are
likely subjected to constant mechanical stress during soil penetration
that could lead to JA production and subsequent detrimental effects on
growth. Our data reveal how distinct negative regulatory layers,
including both NINJA-dependent and -independent mechanisms, restrain JA
responses to allow normal root growth. Mechanistic insights from this
work underline the importance of mapping JA signalling components to
specific cell types in order to understand and potentially engineer the
growth reduction that follows physical damage.